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Mol Genet Genomics. 2015 Dec;290(6):2107-19. doi: 10.1007/s00438-015-1060-4. Epub 2015 May 17.

The phylogeny and evolutionary history of the Lesion Simulating Disease (LSD) gene family in Viridiplantae.

Author information

1
Departamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil.
2
Universidade Estadual do Rio Grande do Sul (UERGS), Santa Cruz do Sul, RS, Brazil.
3
Departamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil. maria.zanettini@ufrgs.br.

Abstract

The Lesion Simulating Disease (LSD) genes encode a family of zinc finger proteins that play a role in programmed cell death (PCD) and other biological processes, such as plant growth and photosynthesis. In the present study, we report the reconstruction of the evolutionary history of the LSD gene family in Viridiplantae. Phylogenetic analysis revealed that the monocot and eudicot genes were distributed along the phylogeny, indicating that the expansion of the family occurred prior to the diversification between these clades. Sequences encoding proteins that present one, two, or three LSD domains formed separate groups. The secondary structure of these different LSD proteins presented a similar composition, with the β-sheets being their main component. The evolution by gene duplication was identified only to the genes that contain three LSD domains, which generated proteins with equal structure. Moreover, genes encoding proteins with one or two LSD domains evolved as single-copy genes and did not result from loss or gain in LSD domains. These results were corroborated by synteny analysis among regions containing paralogous/orthologous genes in Glycine max and Populus trichocarpa. The Ka/Ks ratio between paralogous/orthologous genes revealed that a subfunctionalization process possibly could be occurring with the LSD genes, explaining the involvement of LSD members in different biological processes, in addition to the negative regulation of PCD. This study presents important novelty in the evolutionary history of the LSD family and provides a basis for future research on individual LSD genes and their involvement in important pathway networks in plants.

KEYWORDS:

Gene duplication; LSD family phylogeny; Lesion Simulating Disease (LSD); Protein secondary structure; Synteny; Zinc finger LSD domain

PMID:
25982742
DOI:
10.1007/s00438-015-1060-4
[Indexed for MEDLINE]

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